Step 1 - Pulm 1

denniskwinn's version from 2015-04-25 16:15


Question Answer
Conducting zoneConsists of nose to terminal bronchioles
1) Cartilage is present only in the trachea and bronchi.Brings air in and out.
2)Warms, humidifies, filters air. Anatomic dead pace
3) Walls of conducting airways contain smooth muscle
Respiratory zoneConsists of respiratory bronchioles, alveolar ducts, and alveoli . Participates in gas exchange.
Conducting epithelia1)Pseudostratified ciliated columnar cells extend to the respiratory bronchioles
2)Macrophage clear debris in alveoli
3)Goblet cells extend only to the bronchi
Type I pneumocytes(97% of alveolar surfaces) line the alveoli. Squamous; thin for optimal gas diffusion
Type II pneumocytes(3%) secrete pulmonary surfactant(dipalmitoyl phosphatidylcholine), which ↓ the alveolar surface tension. Cuboidal and clustered. AIso serve a precursors to type I cells and other type II cells.
Type II cells proliferate during lung damage.
Clara cells1)Nonciliated; columnar with secretory granules.
2)Secrete component of surfactant
3)Degrade toxins - act as reserve cells.
4)Can differentiate into type II pneumocytes
(Seen in both Bronchogenic and Bronchoalveolar adenocarcinoma)
5) Have cytochrome p450
Bronchopulmonary segments [setup]1)Each segment has a tertiary (segmental) bronchus and 2 arteries (bronchial and pulmonary) In the center. Arteries run with Airways
2) Veins and lymphatics drain along the borders.
Lecithin-to-sphingomyelin ratio that signifies fetal lung maturity Greater than 2.0


Question Answer
Aspiration While upright-Lower portion of right inferior lobe.Right main bronchus wider and more vertical
Aspiration While supinesuperior portion of right inferior lobe.(closer)
Location of pulmonary arteries to the bronchusRALS - right anterior, left superior [location of what in relation to what?]
Structures perforating the diaphragmIVC at T8
Esophagus, vagus at T10
Aorta(red), thoracic duct (white), azygous vein (blue) at T12
Diaphragm innervationC3,C4,C5 (phrenic nerve) - pain from all the diaphragm can be referred to the shoulder
Muscles used in quiet breathingDiaphragm in inspiration, passive expiration
Muscles used in exercise breathingINSPIRATION: External intercostals, Scalene muscles, Sternomastoids

EXPIRATION: Rectus abdominis, internal and external obliques, transversus abdominis, internal intercostals.


Question Answer
Surfactantdipalmitoyl phosphatidylcholine (lecithin) deficient in neonatal RDS. - produced by type II pneumocytes. . ↓ alveolar surface tension, ↑ compliance, ↓ work of inspiration
Important lung products1. Surfactant 2. Prostaglandins 3. Histamine 4. ACE 5. Kallikrein
Histamine effect↑ bronchoconstriction
ACE effectconverts angiotensin I to angiotensin II - inactivates bradykinin (ACE inhibitors ↑ bradykinin and cause cough, angioedema)
Kallikrein effectactivates bradykinin - which vasodilates (which can→edema→cough)
Physiologic dead space equationTidal volume x ((PaCO2-PexpiredCO2)/PaCO2)
Physiologic dead space =Anatomical dead space of conducting airways + functional dead space in alveoli.
Apex of healthy lung is largest contributor of functional dead space = Volume of inspired air that does not take part in gas exchange.
Hemoglobin T form(taut) form has low affinity for O2
Hemoglobin R form(relaxed) form has high affinity for O2 - (300x). Hemoglobin exhibits positive cooperativity and negative allostery (accounts for the sigmoid O2 dissociation curve for hemoglobin, unlike myoglobin)
Things that shift hemoglobin curve right↑ Cl-, H+, CO2, 2,3-BPG, and temperature


Question Answer
Methemoglobin-Oxidized form of hemoglobin (ferric, Fe3+) that does not bind O2 as readily, but has ↑ affinity for CN-
-Iron in hemoglobin is normally in a reduced state (ferrous, Fe2+)
Methemoglobin treatmentMethylene blue
CN poisoning treatment1)Nitrites (converts some hemoglobin to methemoglobin which binds the CN and allowing cytochrome oxidase to function.
2)Then use thiosulfate to bind this CN-= Renal excreted
3)Then methylene blue to return methemoglobin to normal
CarboxyhemoglobinForm of hemoglobin bound to CO in place of O2 - Causes ↓ oxygen-binding capacity with a left shift in the oxygen-hemoglobin dissociation curve. ↓ oxygen unloading in tissues
-Saturated too early
Pulmonary circulationNormally a low-resistance, high-compliance system. ↓ in PAO2 causes a hypoxic vasoconstriction that shifts blood away from poorly ventilated regions of lung to well-ventilated regions of lung. 1.Perfusion limited - O2 (normal health), CO2, N2O Gas equilibrates early along the length of the capillary, Diffusion can be ↑ only if blood flow ↑ 2. Diffusion limited - gas does not equilibrate by the time blood reaches the end of the capillary
Pulmonary hypertensionNormal pulmonary artery pressure = 10- 14 mmHg; pulmonary hypertenslon > 25 mmHg or > 35 mmHg during exercise. Results in atherosclerosis. medial Hypertrophy, and intimal fibrosis of pulmonary arteries.
Primary pulmonary hypertensiondue to an inactivating mutation in the BMPR2 gene (normal) functions to inhibit vascular smooth muscle proliferation); poor prognosis.
Secondary pulmonary hypertension - due to COPD (destruction of lung parenchyma); mitral stenosis (↑ resistance → ↑ pressure); recurrent thromboemboli (↓ cross-sectional area of pulmonary vascular bed); autoimmune disease (e.g .systemic sclerosis; Inflammation → intimal fibrosis→ medial hypertrophy); left-to-right shunt (↑ shear stress→ endothelial injury); sleep apnea or living at high altitude (hypoxic vasoconstriction).
Course of pulmonary hypertensionsevere respiratory distress → cyanosis and RVH → death from decompensated cor pulmonale


Question Answer
PVR = (Ppulm art - PLatrium) /CO
O2 content = (O2 binding capacity x % saturation) + dissolved O2
Normally 1 g Hb can bind _____ O21.34 mL [O2]
normal Hb amount in blood is 15 g/dL.
Cyanosis results when deoxygenated Hb > 5 g/dL.
Normal O2 binding capacity = 20.1 mL O2/dL.
Arterial PO2 in chronic lung disease [inc/dec & why]↓ because physiologic shunt ↓ O2 extraction ratio.
Oxygen delivery to tissues = cardiac output x oxygen content of blood
PAO2 defalveolar PO2 (mmHg)
PIO2 definspired air O2
PaO2 defarterial PO2
A-a gradientPAO2 - PaO2 - - Normal value is 10-15mmHg, higher gradient may occur in hypoxemia, due to shunting, V/Q mismatch or fibrosis (diffusion block)
PAO2 =can be estimated as 150 - PACO2/0.8 . . Real equation is PIO2 - (PACO2/R) R=respiratory quotient = (CO2 produced/O2 consumed) -


Question Answer
Hypoxemia def↓ PaO2 [definition of]
Hypoxia def↓ O2 delivery to tissue
Ischemia defloss of blood flow [definition of?]
Causes of HypoxemiaHigh altitude (nomral A-a gradient), Hypoventilation (normal A-a gradient), V/Q mismatch (↑ A-a gradient), Diffusion limitation (↑ A-a gradient), Right-to-left shunt (↑ A-a gradient)
Causes of Hypoxia↓CO, Hypoxemia, Anemia, Cyanide poisoning, CO poisonin
Causes of ischemiaImpeded arterial flow, reduced venous drainage
Normal V/Q ratios in lungs1. Apex of lung = 3 (wasted ventilation) 2. Base of lung = 0.6 (wasted perfusion) - in exercise the ratio approaches 1
V/Q = 0airway obstruction (shunt) - 100% O2 does not improve PO2
V/Q = infinityblood flow obstruction (physiologic dead space) - assuming <100% dead space, 100% O2 will improve PO2


Question Answer
Co2 binds to hemoglobin at N terminus of globin - accounts for 5% of CO2 transport in blood
Haldane and Bohr effectoxygenation of Hb promotes dissociation of H+ from Hb. This shifts equilibrium toward CO, formation; therefore, CO2 is released from RBCs (Haldane effect). In peripheral tissue, ↑ H+ from tissue metabolism shifts curve to right, unloading O2 (Bohr)
Co2 transports types1. Bicarbonate (90%), 2. Bound to hemoglobin at N terminus of globin (5%), 3. Dissolved CO2(5%)
Response to high altitudeAcute ↑ in ventilation 2.Chronic ↑ in ventilation. 3. ↑ erythropoietin→ ↑ hematocrit and hemoglobin (chronic hypoxia) 4. ↑ 2,3-DPG (binds to hemoglobin so that hemoglobin releases more O2) 5. Cellular change (↑ mitochondrial) 6. ↑ renal excretion of bicarbonate (e.g., can augment by use of acetazolamide) to compensate for thc respiratory alkalosis 7. Chronic hypoxic pulmonary vasoconstriction results in RVH
Response to exercise1. ↑ CO2 production 2. ↑ O2 consumptlon 3. ↑ ventilation rate to meet O2 demand 4. V/Q ratio from apex to base becomes more uniform 5. ↑ pulm blood flow due to ↑ CO 6. ↓pH during strenuous exercise (2° to lactic acidosis) 7. No change in PaO2 and PaCO2, but ↑ in venous CO2 content
Embolus typesFATBAT - Fat, Air, Thrombus, Bacteria, Amniotic fluid, Tumor - Fat emboli are associated with long bone fractures and liposuction. Amniotic fluid emboli can lead to DIC, especially postpartum,
Pulmonary embolus symptomschest pain, tachypnea, dyspnea
Virchow’s triadPredisposes to DVT - 1. Stasis, 2 Hypercoagulability 3. Endothelial damage
DVT preventionheparin
Homan’s signfast dorsiflexion of the foot - can maybe see DVT (if tender calf muscle w/this)